Atrial and ventricular vulnerability in a patient with the Wolff-Parkinson-White syndrome

An electrophysiologic study was carried out in a patient with the Wolff-Parkinson-White syndrome and a history of spontaneous atrial fibrillation but with no evidence of organic cardiac disease. A single induced premature ventricular depolarization resulted in ventricular tachycardia followed by ventricular fibrillation. Similarly, atrial pacing or premature atrial stimulation resulted in frequent episodes of atrial fibrillation or flutter. The atrial and ventricular effective refractory periods were 180 ms and less than 160 ms, respectively, at a driven cycle length of 480 ms. Intravenous administration of procainamide resulted in lengthening of the refractory periods and failure to induce either atrial or ventricular arrhythmias with pacing. In most patients with enhanced atrioventricular nodal or accessory atrioventricular nodal by-pass, the mechanism of ventricular tachycardia is related to an inordinately rapid ventricular response during supraventricular arrhythmias. In our patient, a unique mechanism was apparent: atrial and ventricular vulnerability to fibrillation was associated with extremely short myocardial effective refractory periods. The relationship of this finding to sudden cardiac death bears further study.